Release of the excitatory neurotransmitter amino acid, glutamate, has been suggested to play a role in ischemic neuronal injury and its contribution to the cumulative injury seen after repeated ischemic insults, was investigated in the gerbil. In vivo microdialysis demonstrated equivalent, transient glutamate release during each of three repeated carotid artery occlusion in continuously anesthetized animals. Parallel studies identified a striking temperature dependence of glutamate release in the physiological range. Recent work has demonstrated a significant postischemic hyperthermia upon release of anesthesia and occlusion in the gerbil model that appears to be an important factor in determining the severity of ischemic injury. Our results suggest that there may be an interaction between temperature and glutamate release after repeated occlusion that could contribute to their cumulative impact under conditions of lasting hyperthermia between ischemic insults.
